These data suggest that TGFβ delivered to the surface of NK-92 cells by AML exosomes engages TGFβRI/II, upregulates SMAD 2/3 phosphorylation, downregulates DAP10 and further downstream, decreases Tbet expression levels, which translates into a loss in NKG2D expression levels and inhibition of cytolytic function in NK-92 cells. This evidence concerns the gene HCST and acute myeloid leukemia.